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CTLA4-IgG ameliorates homocysteine-accelerated atherosclerosis by inhibiting T-cell overactivation in apoE(/) mice
Ma, Kongyang1,2; Lv, Silin1,2; Liu, Bo1,2; Liu, Ziyi1,2; Luo, Yuhong1,2; Kong, Wei1,2; Xu, Qingbo3; Feng, Juan1,2; Wang, Xian1,2
关键词Homocysteine Atherosclerosis Ctla4-igg t Cell Overactivation
刊名CARDIOVASCULAR RESEARCH
2013-02-01
DOI10.1093/cvr/cvs330
97期:2页:349-359
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cardiac & Cardiovascular Systems
研究领域[WOS]Cardiovascular System & Cardiology
关键词[WOS]CD28-DEFICIENT MICE ; SURFACE EXPRESSION ; 2-SIGNAL MODEL ; DEFICIENT MICE ; CD28 ; CTLA-4 ; ACTIVATION ; MECHANISMS ; PATHWAY ; COSTIMULATION
英文摘要

Cytotoxic T lymphocyte antigen 4 (CTLA4) exerts inhibitory effects on T-cell activation by competition with CD28. In this study, we investigated the effect of CTLA4-IgG on homocysteine (Hcy)-induced T-cell activation and potential signal pathways involved in atherosclerotic formation.

The CD28 signal was significantly amplified by Hcy treatment in splenic T cells and hyperhomocysteinaemia (HHcy)-accelerated plaques in apolipoprotein E-deficient (apoE(/)) mice. As a major competitor of CD28, CTLA4-IgG (abatacept) pretreatment, 100 g/week, in apoE(/) mice could reverse 2- and 4-week HHcy-accelerated atherosclerosis. Furthermore, the membrane level of CTLA4 was decreased and the endocytosis level was increased by HHcy. Endocytosed CTLA4 molecules by Hcy were in large vesicles, colocalized with lysosomes and endosomes. Hcy-increased CTLA4 endocytosis and secretion of inflammatory cytokines in T cells were blocked by CTLA4-IgG and the PI3K inhibitor LY294002. Blocking the CD28 signal pathway in T cells significantly decreased Hcy-promoted macrophage migration.

These results illustrate a novel mechanism of CD28-dependent T-cell costimulation involved in HHcy-accelerated atherosclerosis, which extends the pharmacological application of CTLA4-IgG for atherosclerosis.

语种英语
WOS记录号WOS:000313827400019
引用统计
被引频次:26[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/52642
专题北京大学基础医学院
作者单位1.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China
2.Peking Univ, Sch Basic Med Sci, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China
3.Kings Coll London, BHF Ctr, Div Cardiovasc, London SE5 9NU, England
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Ma, Kongyang,Lv, Silin,Liu, Bo,et al. CTLA4-IgG ameliorates homocysteine-accelerated atherosclerosis by inhibiting T-cell overactivation in apoE(/) mice[J]. CARDIOVASCULAR RESEARCH,2013,97(2):349-359.
APA Ma, Kongyang.,Lv, Silin.,Liu, Bo.,Liu, Ziyi.,Luo, Yuhong.,...&Wang, Xian.(2013).CTLA4-IgG ameliorates homocysteine-accelerated atherosclerosis by inhibiting T-cell overactivation in apoE(/) mice.CARDIOVASCULAR RESEARCH,97(2),349-359.
MLA Ma, Kongyang,et al."CTLA4-IgG ameliorates homocysteine-accelerated atherosclerosis by inhibiting T-cell overactivation in apoE(/) mice".CARDIOVASCULAR RESEARCH 97.2(2013):349-359.
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